title: Effect of hydrostatic pressure on ADH induced osmotic water flow in toad bladder.
abstract: The effect of hydrostatic pressure (HP) on antidiuretic hormone (ADH) stimulated osmotic water flow (Jv) across the toad urinary bladder was evaluated. Jv for ADH-stimulated bladders was significantly reduced by an elevation of the serosal HP gradient to 1 cm H2O. Subsequent elimination of the HP gradient resulted in a recovery of Jv. Serosal HP also caused a reversible increase in sucrose permeability (P sucrose). For ADH-treated bladders fixed with glutaraldehyde during serosal HP exposure, subsequent exposure to a mucosal or serosal HP gradient caused acceleration or inhibition of Jv, respectively. The reduction in ADH-associated Jv with serosal HP was apparently caused by a back-flux of water through a paracellular pathway. Jv and P sucrose were not affected by mucosal HP during ADH stimulation. The results suggest a specific sensitivity of a paracellular pathway to a small serosal HP gradient in bladders with ADH-stimulated water flow. The reversibility of this effect on P sucrose suggests that the elements comprising the apical junctions are dynamic structures capable of recovering at least some of their permeability properties.
mesh_terms: D000818:Animals; D001692:Biological Transport; D002024:Bufo marinus; D004848:Epithelium / Q000378:metabolism; D005260:Female; D006874:Hydrostatic Pressure; D009995:Osmosis; D010539:Permeability; D011312:Pressure; D013395:Sucrose / Q000378:metabolism; D001743:Urinary Bladder / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology*; D014867:Water / Q000378:metabolism*
chemical_list: D014867:Water; D014667:Vasopressins; D013395:Sucrose